DNA is renowned for its double helix structure and the base pairing that enables the recognition and highly selective binding of complementary DNA strands. These features, and the ability to create DNA strands with any desired sequence of bases, have led to the use of DNA rationally to design various nanostructures and even execute molecular computations. Of the wide range of self-assembled DNA nanostructures reported, most are one- or two-dimensional. Examples of three-dimensional DNA structures include cubes, truncated octahedra, octohedra and tetrahedra, which are all comprised of many different DNA strands with unique sequences. When aiming for large structures, the need to synthesize large numbers (hundreds) of unique DNA strands poses a challenging design problem. Here, we demonstrate a simple solution to this problem: the design of basic DNA building units in such a way that many copies of identical units assemble into larger three-dimensional structures. We test this hierarchical self-assembly concept with DNA molecules that form three-point-star motifs, or tiles. By controlling the flexibility and concentration of the tiles, the one-pot assembly yields tetrahedra, dodecahedra or buckyballs that are tens of nanometres in size and comprised of four, twenty or sixty individual tiles, respectively. We expect that our assembly strategy can be adapted to allow the fabrication of a range of relatively complex three-dimensional structures.

The fifth generation (5G) wireless communication networks are being deployed worldwide from 2020 and more capabilities are in the process of being standardized, such as mass connectivity, ultra-reliability, and guaranteed low latency. However, 5G will not meet all requirements of the future in 2030 and beyond, and sixth generation (6G) wireless communication networks are expected to provide global coverage, enhanced spectral/energy/cost efficiency, better intelligence level and security, etc. To meet these requirements, 6G networks will rely on new enabling technologies, i.e., air interface and transmission technologies and novel network architecture, such as waveform design, multiple access, channel coding schemes, multi-antenna technologies, network slicing, cell-free architecture, and cloud/fog/edge computing. Our vision on 6G is that it will have four new paradigm shifts. First, to satisfy the requirement of global coverage, 6G will not be limited to terrestrial communication networks, which will need to be complemented with non-terrestrial networks such as satellite and unmanned aerial vehicle (UAV) communication networks, thus achieving a space-air-ground-sea integrated communication network. Second, all spectra will be fully explored to further increase data rates and connection density, including the sub-6 GHz, millimeter wave (mmWave), terahertz (THz), and optical frequency bands. Third, facing the big datasets generated by the use of extremely heterogeneous networks, diverse communication scenarios, large numbers of antennas, wide bandwidths, and new service requirements, 6G networks will enable a new range of smart applications with the aid of artificial intelligence (AI) and big data technologies. Fourth, network security will have to be strengthened when developing 6G networks. This article provides a comprehensive survey of recent advances and future trends in these four aspects. Clearly, 6G with additional technical requirements beyond those of 5G will enable faster and further communications to the extent that the boundary between physical and cyber worlds disappears.

MafA is a transcription factor that binds to the promoter in the insulin gene and has been postulated to regulate insulin transcription in response to serum glucose levels, but there is no current in vivo evidence to support this hypothesis. To analyze the role of MafA in insulin transcription and glucose homeostasis in vivo, we generated MafA-deficient mice. Here we report that MafA mutant mice display intolerance to glucose and develop diabetes mellitus. Detailed analyses revealed that glucose-, arginine-, or KCl-stimulated insulin secretion from pancreatic ␤ cells is severely impaired, although insulin content per se is not significantly affected. MafA-deficient mice also display age-dependent pancreatic islet abnormalities. Further analysis revealed that insulin 1, insulin 2, Pdx1, Beta2, and Glut-2 transcripts are diminished in MafA-deficient mice. These results show that MafA is a key regulator of glucose-stimulated insulin secretion in vivo.Insulin is the only polypeptide hormone that is essential for the regulation of blood glucose levels and is synthesized exclusively in ␤ cells of the islets of Langerhans in the pancreas. The molecular mechanisms that control ␤-cell-specific insulin gene transcription are well characterized. Three conserved cis-regulatory elements within the promoter, E1, A3, and RIPE3b/ C1, respectively, appear to be indispensable for proper insulin gene regulation (22,25). Islet-restricted transcription factors Beta2/NeuroD and Pdx1 bind to the E1 and A3 elements in vitro. Gene disruption experiments in mice have revealed that both Beta2 and Pdx1 play critical roles in insulin gene regulation as well as in islet development and function (1,8,21). Furthermore, mutations in both the Beta2 and Pdx1 genes have been identified within populations of patients with type II diabetes (18,29,30).The third regulatory element, RIPE3b/C1, has also been shown to play a critical role in ␤-cell-specific insulin gene transcription as well as in glucose-regulated expression. Previous studies identified a pancreatic ␤-cell-restricted factor, called the RIPE3b1 activator, that is enriched in response to glucose in pancreatic ␤-cell nuclear extracts. Very recently, four groups reported that the RIPE3b1 activator is a member of the Maf family of transcription factors, MafA (10,12,20,26). The large Maf proteins, MafA/L-Maf/SMaf1 (2, 9, 24), MafB (11), c-Maf (23), and Nrl (31), each contain a basic motif followed by a leucine zipper, and all four family members harbor acidic domains that act as transcriptional activation domains. Although a role for MafA in insulin gene regulation was hypothesized, in vivo tests of the hypothesis have not been reported. To elucidate MafA function in insulin gene regulation, we generated MafA-deficient mice. MATERIALS AND METHODSTargeted disruption of the mafA gene. mafA genomic clones were isolated from a 129/SvJ genomic library (Stratagene) using a partial mouse MafA cDNA as a probe. The targeting vector was constructed with the bacterial lacZ gene containing a nuclear loca...

Nanoparticles can be combined with nucleic acids to programme the formation of three-dimensional colloidal crystals where the particles' size, shape, composition and position can be independently controlled. However, the diversity of the types of material that can be used is limited by the lack of a general method for preparing the basic DNA-functionalized building blocks needed to bond nanoparticles of different chemical compositions into lattices in a controllable manner. Here we show that by coating nanoparticles protected with aliphatic ligands with an azide-bearing amphiphilic polymer, followed by the coupling of DNA to the polymer using strain-promoted azide-alkyne cycloaddition (also known as copper-free azide-alkyne click chemistry), nanoparticles bearing a high-density shell of nucleic acids can be created regardless of nanoparticle composition. This method provides a route to a virtually endless class of programmable atom equivalents for DNA-based colloidal crystallization.